Progress has been slow in identifying genetic factors that influence either susceptibility to IgA nephropathy (IgAN) or its progression to end-stage renal disease (ESRD) [1]. Studies of both familial and sporadic IgAN strongly point to clinical and genetic heterogeneity in the entity we presently call IgAN. The human IgAN phenotype does not exhibit classic Mendelian inheritance patterns, but is better considered using the paradigm for genetically complex human autoimmune diseases, for which multiple loci have been identified by family-based genetic studies. In these complex diseases many different types of genetic variations contribute to the final phenotype. Among the many potential mechanisms involved, interest has recently been focused on specific single-nucleotide polymorphism (SNP) alleles that alter the transcriptional activity of genes involved in the pathogenesis. Recently, it has been said that 30–50% of human genes with coding SNPs can present allelic variation in gene expression [2].